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  http://www.lef.org/    Life Extension Magazine April 2013 Misconceptions About Atherosclerosis By William Faloon Atherosclerosis  is the underlying cause of most heart attacks and strokes, yet doctors remain confused as to how this artery - blocking process occurs. Most cardiologists overlook specific mechanisms that inflict arterial wall damage and the ensuing progression to occlusive atherosclerotic disease. The result is that only a few of the factors that accelerate arterial blockage (such as elevated LDL) are addressed in today’s clinical setting. Doctors think of an atherosclerotic lesion as a “ clog ” consisting of fat, cholesterol, and platelets that have accumulated on an inner arterial wall. As a result, they tell their patients to eat less fat, take a statin drug (if cholesterol levels are high), and use a baby aspirin to prevent arterial platelet aggregation. The problem with these approaches is that while they may postpone a heart attack or stroke, they fail to correct the underlying pathologies that cause atherosclerotic lesions to form and progress. If people are to live long lives free of the ravages of atherosclerosis, these lethal misconceptions must be cleared up. Otherwise, there will be an epidemic of aging people receiving coronary stents, undergoing bypass surgeries, and dropping dead from sudden heart attacks. WHY ARTERIES CLOG AS WE AGE   The aging process damages blood vessels, even when conventional risk factors such as cholesterol and blood pressure are within normal ranges. For over 40 years, the standard treatment for coronary atherosclerosis has been to bypass the blocked arteries. Recuperation from this procedure can take months, and some patients are afflicted with lifetime impairments such as chronic inflammation, memory loss, and depression. 1-11  Stenting open narrowed coronary arteries has become prevalent over the past decade, but this procedure is not a cure for underlying systemic endothelial dysfunction and atherosclerosis. A review of the scientific literature reveals that atherosclerosis is associated with high blood levels of homocysteine, 12-14   fibrinogen, 15-18  C - reactive protein, 12,15,19-26  glucose, 27,28  cholesterol, 29-32  insulin, 33-36  iron, 37-40  LDL, 41-44  and triglycerides, 45-48  along with low levels of HDL 49-52  and testosterone (in men). 53-58  Optimizing blood levels of these substances can dramatically reduce heart attack and stroke risk. Despite thousands of studies validating that atherosclerosis is a multifactorial process, today’s doctors often prescribe a statin drug as the sole therapy to prevent and treat coronary atherosclerosis. Mainstream cardiologists fail to appreciate that coronary atherosclerosis is a sign of systemic arterial dysfunction requiring aggressive therapy to correct. ANATOMY OF THE ARTERY  Arteries are the blood vessels that bear the full force of each heartbeat. Most people think of arteries as flexible tubes whose only function is to carry blood that flows continuously throughout the body. In fact, arteries are dynamic, functioning muscular structures that, when healthy, expand and contract to facilitate circulation and maintain optimal blood pressure. The outer layer of the artery comprises mostly connective tissue and provides structural containment for the two layers beneath. The middle area comprises elastic smooth muscle that provides the contractile strength to make possible the artery’s expansion and contraction with each heartbeat. The inner layer, known as the endothelium , comprises a thin area of endothelial cells whose integrity is crucial if atherosclerosis is to be prevented. Poor health habits and normal aging result in endothelial dysfunction  , a process in which the endothelium boundary is broken, arterial flexibility is diminished, abnormal platelet aggregation occurs, and atherosclerotic lesions form in response to arterial wall (endothelium) injuries. HOW DO MOST HEART ATTACKS AND STROKES OCCUR?   The two prime factors involved in occlusive arterial disease are abnormal platelet aggregation and endothelial dysfunction  . When the endothelium is not functioning properly, our platelets (blood - clotting cells) become dangerously over - activated. This can cause a sudden arterial blood clot, or contribute to progression of atherosclerosis by stimulating inflammation. A primary mechanism involved in endothelial dysfunction   is the depletion of nitric oxide , often caused from the oxidation of LDL and other blood components. Nitric oxide is produced by endothelial cells. It regulates vascular elasticity, maintains cardiac contraction, prevents vessel injury, and helps protect against atherosclerosis. 59-62  As humans age, endothelial function becomes altered. Due to a variety of insults, a depletion of nitric oxide occurs in the endothelium. One consequence of nitric oxide depletion  is the inability of arteries to expand and contract with youthful elasticity. The continual stiffening and occlusion of aged arteries is the number one health risk that people in Western societies face. 63-68  In order to maintain healthy arterial dilation, the endothelium has to manufacture enough nitric oxide . Impairment in nitric oxide release by the aging endothelium causes arterial dysfunction. 69,70  Therapies used by today’s mainstream cardiologists (aspirin, statin, and certain anti - hypertensive drugs) have a beneficial effect on the endothelium, but they may only postpone a serious vascular event. If a person lives long enough, the chronic depletion of endothelial nitric oxide   results in impairment of arterial function and progressive restriction of blood flow to vital parts of the body. WHAT YOU NEED TO KNOW Guard Against Lethal Medical Misconceptions n Doctors think of an atherosclerotic lesion as a “ clog ” consisting of fat, cholesterol, and platelets that have accumulated on an inner arterial wall. n Despite thousands of studies validating that atherosclerosis is a multifactorial process, today’s doctors often prescribe a statin drug as the sole therapy to prevent and treat coronary atherosclerosis. n Stenting open narrowed coronary arteries has become prevalent over the past decade, but this procedure is not a cure for underlying systemic endothelial dysfunction and atherosclerosis. n The aging process damages blood vessels, even when conventional risk factors such as cholesterol and blood pressure are within normal ranges. n A review of the scientific literature reveals that atherosclerosis is associated with high blood levels of homocysteine, fibrinogen, C - reactive protein, glucose, cholesterol, insulin, iron, LDL, and triglycerides, along with low levels of HDL and testosterone (in men). n Poor health habits and normal aging result in endothelial dysfunction, a process in which the endothelium boundary is broken, arterial flexibility is diminished, abnormal platelet aggregation occurs, and athero - sclerotic lesions form in response to arterial wall (endothelium) injuries. n A primary mechanism involved in endothelial dysfunction is the depletion of nitric oxide, often caused from the oxidation of LDL and other blood components. n Annual blood testing is critical to identifying one’s individual risk factors.  SUMMARY Endothelial cells  line the arteries, veins, arterioles, and capillaries of the vascular system. Doctors used to view the endothelium as a relatively inert structure that played no active role in vascular function. Starting around 20 years ago, research has shown that the endothelium is dynamic and participates in vital aspects of arterial structure and function. 74   Over the years, Life Extension   ® has reported on advances related to protecting the endothelium against age - related deterioration, such as the remarkable ability of pomegranate  to reverse clinical measurements of systemic atherosclerosis (in both carotid and coronary arteries). 75-81  A typical 50 - year - old human can postpone a major cardiovascular event by following relatively simple steps, such as eating healthy and taking a low - dose statin drug if LDL is over 100 mg/dL . As that same person ages, however, multiple processes involved in endothelial dysfunction   too often manifest in the form of a vascular - related disorder. Endothelial cells that line blood vessels are crucial to maintaining vascular integrity. Endothelial dysfunction   is a critical factor in the initiation and progression of cardiovascular disease, 82-84  yet mainstream doctors continue to ignore this dominant underlying cause of arterial occlusion. Pomegranate  extracts protect against endothelial dysfunction   via several well - defined mechanisms, including protection of vital endothelial nitric oxide . 85-87  Atherosclerosis remains the number - one cause of death and disability in the United States. 88  The graphic on the next page shows 17 independent risk factors of atherosclerosis , with low EPA/DHA blood levels being only one of the elements that must be controlled if heart attack and ischemic stroke are to be averted. Annual blood testing  is critical to identifying one’s individual risk factors. Modest - dose fish oil alone will not reverse the endothelial dysfunction that exists in aging humans with preexisting atherosclerosis. To read specifically how atherosclerosis initiates and progresses, refer to the next article. If you have any questions on the scientific content of this article, please call a Life Extension  ® Health Advisor at 1 - 866 - 864 - 3027 . WHY SOME ELDERLY PEOPLE NEED MORE THAN A STATIN DRUG Did you know that popular “ statin ” drugs used to reduce LDL and cholesterol often lose their ability to protect against vascular disease as people age? 71-73  The reason is simple. Aging arteries are subjected to more destructive forces than blood vessels of young people. Statins have shown beneficial effects to the endothelium in addition to reducing cholesterol and LDL. As we age, however, we must go beyond basic therapies (such as statin drugs) that may have protected us in younger years. Prevention of the epidemic of stroke and heart disease in the elderly requires that we aggressively counteract the underlying causes of endothelial dysfunction. Some people require the proper dose of statin drug to control excess cholesterol - LDL, but all aging humans need to take assertive actions to protect their precious endothelium against the functional and structural distortions that lead to arterial occlusion.    This image depicts daggers aimed at an artery occluded with atherosclerotic plaque. Any one of these “ daggers ” can initiate and propagate vascular disease. In the real world, aging humans suffer small pricks from the point of these daggers over a lifetime. The cumulative effect of these dagger pricks (risk factors) is arterial occlusion and, far too often, stroke or acute heart attack. REFERENCES 1.Suksompong S, Prakanratrana U, Chumpathong S, Sriyoschati S, Pornvilawan S. Neuropsychological alterations after coronary artery bypass graft surgery. J Med Assoc Thai  . 2002 Sep;85 Suppl 3:S910 - 6. 2.Strauss B, Paulsen G, Strenge H, Graetz S, Regensburger D, Speidel H. Preoperative and late postoperative psychosocial state following coronary artery bypass surgery. Thorac Cardiovasc Surg  . 1992 Apr;40(2):5964. 3.Scholz M, Nowak P, Blaheta R, et al. Relocalization of endothelial cell betacatenin after coculture with activated neutrophils from patients undergoing cardiac surgery with cardiopulmonary bypass. Invest Surg  . 2004 May - Jun;17(3):143 - 9. 4.Dacey LJ, DeSimone J, Braxton JH, et al. Preoperative white blood cell count and mortality and morbidity after coronary artery bypass grafting. Ann Thorac Surg.  2003 Sep;76(3):760 - 4. 5.Wei M, Kuukasjarvi P, Laurikka J, et al. Relation of cytokines to vasodilation after coronary artery bypass grafting. World J Surg  . 2003 Oct;27(10):1093 - 8. 6.Bergh C, Backstrom M, Jonsson H, Havinder L, Johnsson P. In the eye of both patient and spouse: memory is poor 1 to 2 years after coronary bypass and angioplasty. Ann Thorac Surg  . 2002 Sep;74(3):689 - 93. 7.Fearn SJ, Pole R, Wesnes K, Faragher EB, Hooper TL, McCollum CN. Cerebral injury during cardiopulmonary bypass: emboli impair memory. J Thorac Cardiovasc Surg  . 2001 Jun;121(6):1150 - 60.
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